简单的机械线索可以解释脂肪组织形态
Simple mechanical cues could explain adipose tissue morphology
摘要：
器官获得其功能结构并随着时间的推移实现其维持（或稳态）的机制在很大程度上仍然未知。在本文中，我们调查这个问题的脂肪组织。脂肪组织可占体重的20 - 50%。它的研究是克服严重打击全球人口的大量代谢紊乱的关键。脂肪组织由脂肪细胞的小叶簇组成，周围有组织的胶原纤维网络。通过提供脂肪生成所需的底物，血管系统被认为诱导毛细血管末端附近的脂肪细胞的重组。本文表明，这些结构的出现可以解释为简单的机械相互作用之间的脂肪细胞和胶原纤维。我们的假设是，纤维网络抵抗由生长的脂肪细胞引起的压力，并迫使它们重组成簇。反过来，细胞簇迫使纤维合并成组织良好的网络。我们验证了这一假设的装置的二维个人为基础的模型（IBM）的相互作用的脂肪细胞和细胞外基质纤维元素。该模型产生的结构，比较定量以及实验观察。我们的模型似乎表明，细胞簇可以自发地出现，作为细胞和纤维之间的简单机械相互作用的结果，令人惊讶的是，这些结构的出现并不直接需要脉管系统。
英文摘要：
The mechanisms by which organs acquire their functional structure and realize its maintenance (or homeostasis) over time are still largely unknown. In this paper, we investigate this question on adipose tissue. Adipose tissue can represent 20 to 50% of the body weight. Its investigation is key to overcome a large array of metabolic disorders that heavily strike populations worldwide. Adipose tissue consists of lobular clusters of adipocytes surrounded by an organized collagen fiber network. By supplying substrates needed for adipogenesis, vasculature was believed to induce the regroupment of adipocytes near capillary extremities. This paper shows that the emergence of these structures could be explained by simple mechanical interactions between the adipocytes and the collagen fibers. Our assumption is that the fiber network resists the pressure induced by the growing adipocytes and forces them to regroup into clusters. Reciprocally, cell clusters force the fibers to merge into a well-organized network. We validate this hypothesis by means of a two-dimensional Individual Based Model (IBM) of interacting adipocytes and extra-cellular-matrix fiber elements. The model produces structures that compare quantitatively well to the experimental observations. Our model seems to indicate that cell clusters could spontaneously emerge as a result of simple mechanical interactions between cells and fibers and surprisingly, vasculature is not directly needed for these structures to emerge.
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